DESCRIPTION (applicant's abstract): Human CMV (HCMV) is an important human pathogen. Most HCMV infections are asymptomatic; however, they are much more serious in fetuses, neonates, and immunosuppressed adults, including patients with the acquired immune deficiency syndrome. Cytomegalic inclusion disease results in birth defects affecting the nervous system, including blindness, deafness and microcephaly. HCMV has also been associated with the reticuloendothelial tumor, Kaposi's sarcoma. The most effective approach to treat, and ultimately prevent, CMV retinopathy is to explore an experimental model of CMV retinitis. Unfortunately, no experimental model of the acquired immune deficiency syndrome exists in the rodent, although it may be achieved in the near future. Nevertheless, important information concerning the pathophysiology and treatment of CMV retinopathy, in either of the two currently-defined models of experimental murine CMV (MCMV) retinitis can now be obtained. The applicant, therefore, proposes the following: 1) to refine the experimental models of MCMV retinitis; 2) to investigate the pathogenesis of experimental MCMV retinitis; 3) to study the systemic immune response in experimental MCMV retinitis; and 4) to investigate medical therapy in experimental MCMV retinitis.